The major objective of of this project is to evaluate tissue damage resulting fromtraumatic brain injury (TBI) utilizing non-invasive NMR techniques. We have previously shown that the the quantitative perfusion imaging technique using arterial spin labeling developed at this Center is particularly useful for studying blood flow changes in a TBI model. The ability to evaluate the effect of therapies on cerebrovascular dynamics in has been very restricted due to limitations of previous evaluation methodologies. For example, optimal manipulation of arterial pCO2 in TBI remains controversial in a clinical setting. The specific aim of the present study is to monitor the CO2 reactivity from serial MRI perfusion maps, in order to understand the effects of arterial pCO2 manipulation in a severe TBI model. Cerebral perfusion images of a group of rats, 24 hours post-TBI were measured in a coronal plane through the injured region using the arterial spin labeling technique. TBI was produced by controlled cortical impact in the left hemisphere. Perfusion images were first obtained with ventillation controlled to give an arterial pCO2 of 30-40 mmHg, and then repeated with the ventillation adjusted to give an arterial pCO2 of 15-25 mm Hg. The experiments were repeated on a control group of rats with no TBI. Cerebral blood flow (CBF) was measured in a region of interest covering the TBI, and in a comparable region in the control rats. During normal ventillation, mean perfusion values within the left cortex were 117 and 245 ml 100g-1 min -1 in the trauma and normal groups, respectively. Hyperventillation reduced mean CBF to 75-117 ml 100g-1 min -1 in the trauma group and 119-245 ml 100g-1 min -1 in the control group. These results suggest that TBI results in an attenuation of the CO2 reactivity in the injured cortex. Careful inspection of the perfusion maps also indicate that the CO2 reactivity is completely lost in contusion area. To our knowledge, these studies represent the first assessment of CO2 reactivity after TBI in a rodent model.